Activity in eye surface sensory neurons is disturbed by inflammation, and vice versa

• Published in: Acta ophthalmologica (Oxford, England) Vol. 95; no. S259
• Main Authors: Gallar, J., Acosta, M.C.
• Format: Journal Article
• Language: English
• Published: Malden Wiley Subscription Services, Inc 01.09.2017
• Subjects: Axons; Blindness; Blinking; Excitability; Eye; Inflammation; Membrane channels; Metabolic disorders; Nerve endings; Neurons; Neuropeptides; Nociceptors; Pain; Pain perception; Peripheral neuropathy; Regeneration; Sensory neurons; Stimulation; Surgery; Tearing; Thermoreceptors; Tissues; Trauma; Trigeminal ganglion
• ISSN: 1755-375X; 1755-3768
• DOI: 10.1111/j.1755-3768.2017.03141

Summary Ocular pain results from noxious stimulation of peripheral axons of functionally heterogeneous (Mechanonociceptors, polymodal nociceptors, and cold thermoreceptors) trigeminal ganglion neurons whose sensitivity to different stimulating agents depends on the expression of specific classes of membrane channels, evoking also different pain sensations. Inflammatory mediators increase the excitability (sensitization) of ocular polymodal nociceptors, enhancing pain sensations. In turn, excited polymodal nociceptors release locally neuropeptides, contributing to local inflammatory reaction (neurogenic inflammation). However, inflammatory mediators reduce the excitability of cold thermoreceptors. Regenerating nerve terminals damaged by ocular surgery, trauma, infections or systemic metabolic diseases, develop spontaneous activity and abnormal responses to natural stimulation, inducing changes in the experienced sensations (dysesthesia, neuropathic pain), and disturbances in tearing, blinking and ocular surface trophism. Besides, ocular tissues provide molecular signals that increase nerve regeneration. (Supported by ARREST‐BLINDNESS, GA No. 667400‐2, Horizon 2020‐EC, and in part by SAF2014‐54518‐C3‐1‐R, MINECO, Spain and FEDER‐EC)